The control of fetal lung development was investigated by studying the effects of several factors, including insulin, morphine sulfate and prostaglandin production, on the synthesis and secretion of lamellar bodies. A new method of measuring insulin receptors in fetal lung was developed. The number of insulin receptors per cell was found to increase 6-fold during the last trimester in fetal rat lungs. Administration of morphine sulfate to pregnant rats caused a significant acceleration of fetal lung development as assessed by both morphological criteria and lecithin/sphingomylin ratios. The first step in prostaglandin biosynthesis, the hydrolysis of arachidonic acid from phosphatidylcholine was shown to be stimulated by calcium ionophore, suggesting a role for calcium in the production of prostaglandins and the production of disaturated phosphatidylcholine. In conjunction with the prostaglandin studies, an imbalance in platelet thromboxane and vascular prostacyclin was demonstrated in vitro in the presence of homocysteine and homocystine, substances elevated in homocystinuria, a disorder of sulfur metabolism.